Since the 1980s, molecular hypotheses attributing general anesthesia to nonspecific membrane biophysical perturbations have largely receded, while researchers have embraced the idea that anesthetic drugs act directly at protein targets, that is, classical receptors. However, there is little evidence supporting this hypothesis for volatile anesthetics. Pandit et al. in this volume of Anesthesiology add another piece to the challenging puzzle of volatile anesthetic mechanisms.

The new work by Pandit et al. relates clinically to a toxic effect of volatile anesthetics: inhibition of the hypoxic ventilatory response. Loss of this important physiologic reflex may contribute to postoperative hypoventilation, hypoxia, and associated morbidity. In the neural circuits underlying the hypoxic ventilatory response, glomus type I cells located in the carotid bodies and aortic bodies are the sensory cells, and their molecular chemosensing elements include...

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